Conclusion
We found that lincROR expression was significantly inhibited because of the increased concentration of crizotinib in EML4-ALK+ NSCLC cells. Furthermore, lincROR overexpression increased cell viability of EML4-ALK+ NSCLC cells, which was impaired by crizotinib. Conjointly, these results suggested the important role of lincROR in EML-ALK+ NSCLC. lincROR may serve as a potential therapeutic target to overcome chemotherapy resistance in EML-ALK+ NSCLC.
Methods
In the present study, we investigated the expression profile of lincROR in EML-ALK NSCLC tissues, and the potential role of lincROR in prognosis was then analyzed. Subsequently, its association with stem cell-like properties of EML-ALK+ NSCLC cells was determined. Furthermore, the correlation of lincROR with crizotinib and the effects of lincROR and crizotinib on cell viability of EML4-ALK+ NSCLC cells were all explored.
Results
The results showed that lincROR expression was upregulated in EML4-ALK+ NSCLC tissues relative to EML4-ALK- NSCLC tissues. Low-expressed lincROR was related to a favorable prognosis of patients with EML-ALK NSCLC. lincROR overexpression could enhance the stemness features of EML-ALK+ NSCLC cells which were repressed by ALK knockdown.